There are two main research lines within the NAVI-group: The Neuro-Aging team (PI: Ann Massie) and the Viro-Immunology team (PI: Joeri Aerts).
Ann Massie's Neuro-Aging team focuses on glutamate transport, with emphasis on system xc-, in health and disease.
We have ongoing projects on the role of system xc- or the cystine/glutamate antiporter in e.g. Parkinson’s disease, Alzheimer’s disease, and (central effects of) (pancreatic) cancer. Our overall hypothesis that inhibition of system xc- might be a therapeutic strategy to treat (age-related) diseases that are characterized by excitotoxicity and neuroinflammation, also necessitates research towards the importance of system xc- in normal (healthy) brain functioning. As such, we are investigating how system xc- regulates glutamatergic transmission and plasticity under physiological conditions. Finally, we study the involvement of system xc- in the process of (brain) aging. To increase the translational value of this research, we actively search for novel strategies to target system xc-.
Joeri Aerts' Viro-immunology team can be divided in two parts.
The first part focuses on the development of novel immunotherapeutic approaches for the treatment of HIV infections. We have a longstanding expertise in this field, with a special focus on raising strong T cell responses to keep the virus at bay. We are now investigating mRNA and self-replicating RNA packaged by state-of-the-art nanoparticle systems for optimal delivery in patients. A major bottleneck for this type of research is the presence of a latent reservoir, consisting of resting immune cells that harbor the HIV virus in their genome. The possibility to target latently infected cells by stimulating various aspects of the immune system, with a special focus on natural killer cells, is being investigated.
The second part of our research is focused on immunogenic cell death in cancer cells and how this can contribute to enhanced anti-tumor responses. Viruses have the unique capacity to outsmart tumor cells by exploiting mechanisms that are used to transform normal cells (e.g. a reduced type 1 interferon production capacity). Based on this principle so-called oncolytic viruses, can replicate exclusively in tumor cells, but not in healthy cells. We want to explore how oncolytic viruses can be modified in order to increase immunogenic cell death, thus enhancing their anti-tumor immune responses.